Abstract
To test the hypothesis that the Ca 2+ channel blocker mibefradil slows heart rate due to inhibition of T-type Ca 2+ current in pacemaker cells, we studied effects of mibefradil on action potentials and ionic currents of isolated rabbit sinus node cells using the patch clamp technique. Mibefradil (100 nM and 1 μM) reduced spontaneous rate, decreased action potential amplitude and finally stopped impulse initiation. This action was not due to the drug effect on hyperpolarization-activated pacemaker current, but can be explained by attenuation of both T- and L-type Ca 2+ currents, which were inhibited by mibefradil almost equally (55% and 64% inhibition with 1 μM for T- and L-types, respectively).
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